DIABETES MELLITUS

Signs and SymptomsTYPE 1 DIABETES10% of all cases of diabetes are type 1diagnosed before the age of 40

caused by a T cell–mediated autoimmune destruction of beta cells in the pancreas.

At least 80% to 90% of beta cell function must be lost before hyperglycemia occurs.

presentation is ofen sudden and severe hyperglycemia over several days to weeks associated with fatigue, weight loss, polyuria, polydipsia, blurring of vision, and signs of intravascular volume depletion .

diagnosis is based on the presence of a random blood • BS more than 200 mg/dL • Hb A1c level of more than 7.0%. • Te presence of ketoacidosis TYPE 2 DIABETES90% of all cases of diabetes mellitus in the world.the middle to older age group

Type 2 diabetes is characterized by relative beta cell insuffciency and insulin resistance

Tree important defects :

(1 )an increased rate of hepatic glucose release

(2 )impaired basal and stimulated insulin secretion

( 3 )inefcient use of glucose by peripheral tissues (i.e., insulin resistance)

Impaired glucose tolerance is associated with an increase in body weight, a decrease in insulin secretion, and a reduction in peripheral insulin action.

Metabolic syndrome : combines insulin resistance with hypertension, dyslipidemia, a procoagulant state, and obesity, and is associated with premature atherosclerosis and subsequent cardiovascular disease.

Diagnosisupper limit for normal fasting glucose level is 100 mg/dL.70-100

Any fasting glucose level between 101 and 125 mg/dL is impaired fasting glucose.

The Hb A1c test provides a valuable measure of long-term glycemic control 60-90 days.

The normal range for Hb A1c is 4% to 6%.

Treatmenttype 2 diabetes are dietary With weight loss, exercise therapy, and oral antidiabetic drugs.

Oral agents:

Hypoglycemia is the most common side efect.

sulfonylureas :ATP channels in the myocardium mediate ischemic preconditioning, which results in larger myocardial infarction areas.

Not only must hyperglycemia be treated but all abnormalities of insulin resistance (metabolic syndrome) must be managed, with the goals of therapy including an Hb A1c level of less than 7%, a low-density lipoprotein level of less than 100 mg/dL, a high-density lipoprotein level of more than 40 mg/dL in men and more than 50 mg/dL in women, a triglycerides level of less than 200 mg/dL, and a blood pressure of less than 130/80 mm Hg.

INSULIN

type 1 diabetes and 30 % of patients with type 2 diabetes

total daily basal dose of insulin equals ( weight × 0.3), with the hourly rate obtained by dividing by 24.

Hypoglycemia is the most frequent and dangerous complication of insulin therapy.

exacerbated by simultaneous administration of alcohol, sulfonylureas, biguanides, thiazolidinediones, angiotensin-converting enzyme (ACE) inhibitors, monoamine oxidase inhibitors, and nonselective β-blockers.

. Hypoglysemia The diagnosis in adults requires a plasma glucose level of less than 50 mg/dL.

Symptoms are adrenergic (sweating, tachycardia, palpitations, restlessness, pallor) and neu-roglycopenic (fatigue, confusion, headache, somnolence, convulsions, coma).

Treatment includes the administration of sugar and

glucose 0.5 g/kg IV

glucagon 0.5 to 1.0 mg IV, IM, or SC

Complications

1.DIABETIC KETOACIDOSISDiabetic ketoacidosis (DKA) is a complication of decompensated diabetes mellitus.

signs and symptoms of DKA are primarily the result of abnormalities in carbohydrate and fat metabolism.

Episodes of DKA occur more commonly in patients with type 1 diabetes and are precipitated by infection or acute illness.

signifcant osmotic diuresis with marked hypovolemia.

DKA results in an excess of glucose counterregulatory hormones, with glucagon activating lipolysis and free fatty acids providing the substrate for ketogenesis.

An increase in production of ketoacids (β-hydroxybutyrate, acetoac-etate, acetone) creates an anion gap metabolic acidosis. Substantial defcits of water, potassium, and phosphorus exist, although laboratory values of these electrolytes may be normal or increased. Hyponatremia results from the efect of hyperglycemia and hyperosmolarity on water distribution. Te defcit of potassium is usually substantial (3 to 5 mEq/kg), and the defcit of phosphorus can lead to diaphragmatic and skeletal muscle dysfunction and impaired myocardial contractility.

The treatment of DKA consists administration of large amounts of normal saline

efective doses of insulin

electrolyte supplementation.

1-intravenous loading dose of 0.1 unit/kg of regular insulin plus a low-dose insulin infusion of 0.1 unit/kg/hr is initiated.

2-Insulin administration must be continued until a normal acid-base status is achieved.

3-The insulin rate is reduced when hyperglycemia is controlled, the blood pH is higher than 7.3, and bicarbonate level is more than 18 mEq/L.

4- Potassium and phosphate are replaced with KCl and K2PO4.

5-Magnesium is replaced as needed.

6-Sodium bicarbonate is administered if the blood pH is less than 7.1.

cerebral edema can result from correction of hyperglycemia without simultaneous correction of serum sodium level.

The overall mortality rate from DKA is 5% to 10%,

HYPERGLYCEMIC HYPEROSMOLAR SYNDROME Hyperglycemic hyperosmolar syndrome is characterized by severe

hyperglycemia, hyperosmolarity, and dehydration. It usually occurs in patients with type 2 diabetes who are older than 60 years

of age in the context of an acute illness.

The syndrome evolves over days to weeks with a persistent glycosuric diuresis.

When the glucose load exceeds the renal tubular maximum for glucose reabsorption, a massive solute diuresis occurs with total body water depletion.

Te patient experiences polyuria, polydipsia, hypovolemia, hypotension, tachycardia, and organ hypoperfusion. Hyperosmolarity (>340 mOsm/L) is responsible for mental obtundation or coma.

Treatment : includes signifcant fluid resuscitation, insulin administration, and electrolyte supplementation.

1- If the plasma osmolarity is greater than 320 mOsm/L, large volumes of hypotonic saline (1000 to 1500 mL/hr) should be administered until the osmolarity is less than 320 mOsm/L, at which time large volumes of isotonic saline (1000 to 1500 mL/hr) can be given.

2- Insulin therapy is initiated with an intravenous bolus of 15 units of regular insulin followed by a 0.1 unit/kg/hr infusion. Te insulin infusion is decreased to 2 to 3 units/hr whenthe glucose level decreases to approximately 250 to 300 mg/dL.

The mortality rate of hyperglycemic hyperosmolar syndrome is 10% to 15%.

MICROVASCULAR COMPLICATIONS

nephropathy

The clinical course is characterized by hypertension, albuminuria, peripheral edema, and a progressive decrease in glomerular fltration rate.

When the glomerular fltration rate decreases to less than 15 to 20 mL/min, the ability of the kidneys to excrete potassium and acids is impaired and patients develop hyperkalemia and metabolic acidosis.

Hypertension, hyperglycemia, hypercholesterolemia, and microalbuminuria accelerate the decrease in the glomerular fltration rate.

Treatment of hypertension can markedly slow the progression of renal dysfunction. ACE inhibitors are particularly benefcial in diabetic patients because they retard the progression of proteinuria and the decrease in glomerular fltration rate.

Peripheral Neuropathy

A distal symmetric diffuse sensorimotor polyneuropathy is the most common form.

"stocking and glove" distribution.

Retinopathy

Diabetic retinopathy results from a variety of microvascular changes

Strict glycemic control and blood pressure control can reduce the risk of development and progression of retinopathy.

Autonomic Neuropathy

Symptomatic autonomic neuropathy is rare and is present in fewer than 5% of diabetics.

Diabetic autonomic neuropathy can afect any part of the autonomic nervous system and is the result of damaged vasoconstrictor fibers, impaired baroreceptor function, and ineffective cardiovascular reactivity.

Resting tachycardia and loss of heart rate variability during deep breathing.

A heart rate that fails to respond to exercise is indicative of signifcant cardiac denervation and is likely to result in substantially reduced exercise tolerance. .

systolic and diastolic dysfunction with a reduced ejection fraction. Dysrhythmias may be responsible for sudden death. In advanced stages, severe orthostatic hypotension is present

The presence of cardiovascular autonomic neuropathy can be demonstrated by measuring

orthostatic changes in heart rate and blood pressure and the hemodynamic response to exercise.

symptomatic patients will have nausea, vomiting, early satiety, bloating, and epigastric pain. Treatment of gastroparesis includes strict blood glucose control, consumption of multiple small meals, reduction of the fat content of meals, and use of prokinetic agents such as metoclopramide.

Diarrhea and constipation are also common among diabetic patients and may be related to diabetic autonomic neuropathy.

Management of Anesthesia PREOPERATIVE EVALUATION

1. the preoperative evaluation should emphasize the cardiovascular, renal, neurologic, and musculoskeletal systems.

2. The index of suspicion should be high for myocardial ischemia and infarction. Silent ischemia is possible if autonomic neuropathy

3. autonomic neuropathy predisposes the patient to perioperative dysrhythmias and intraoperative hypotension.

4. Preoperative evaluation of the musculoskeletal system should look for limited joint mobility caused by nonenzymatic glycosylation

 

1. Firm, woody, nonpitting edema of the posterior neck and upper back (scleredema of diabetes) coupled with impaired joint mobility may limit range of motion of the neck and render endotracheal intubation difcult.

2. Gastroparesis may increase the risk of aspiration

Management of insulin in the preoperative period.

If a patient takes subcutaneous insulin each night at bedtime, two thirds of this dose (NPH and regular) should be administered the night before surgery, and one half of the usual morning NPH dose should be given on the day of surgery. The daily morning dose of regular insulin should be held

If the patient uses an insulin pump, the overnight rate should be decreased by 30%.

  Oral hypoglycemics should be discontinued 24 to 48 hours

preoperatively.

  It is advised that sulfonylureas be avoided during the entire

perioperative period, because they block the myocardial potassium ATP channels that are responsible for ischemia and anesthetic-induced preconditioning.

 

INTRAOPERATIVE MANAGEMENT

Aggressive glycemic control is important intraoperatively .

Ideally, a continuous infusion of insulin should be initiated at least 2 hours before surgery.

Intraoperative serum glucose levels should be maintained between 120 and 180 mg/dL.

Levels above 200 mg/dL are likely to cause glycosuria and dehydration and to inhibit phagocyte function and wound healing.

Typically, 1 unit of insulin lowers glucose approximately 25 to 30 mg/dL.

A typical rate is 0.02 unit/kg/hr.

An insulin infusion can be prepared by mixing 100 units of regular insulin in 100 mL of normal saline (1 unit/mL).

Insulin infusion requirements are higher or patients undergoing

coronary artery bypass graf surgery

patients receiving steroids

patients with severe infection

patients receiving hyperalimentation

patients receiving vasopressor infusions

An insulin infusion should be accompanied by an

1. infusion of 5%dextrose in

2. half-normal saline

3. 20 mEq KCl

4. at 100 to 150 mL/hr

Serum glucose level should be monitored at least every hour and even every 30 minutes in patients undergoing coronary artery bypass surgery or patients with high insulin requirements.

Urine glucose monitoring is not reliable.

Avoidance of hypoglycemia is especially critical, since recognition of hypoglycemia may be delayed in patients receiving anesthetics, sedatives, analgesics, β-blockers, or sympatholytics and in those with autonomic neuropathy.

If hypoglycemia does occur, treatment consists of administration of 50 mL of 50% dextrose in water, which typically increases the glucose level 100 mg/dL or 2 mg/dL/mL.

INSULINOMA

Tumors of pancreatic beta cell.

Insulinomas are rare and benign.

Tey usually occur as an isolated fnding but may present as part of multiple endocrine neoplasia syndrome type I (insulinoma, hyperparathyroidism, and a pituitary tumor).

Profound hypoglycemia can occur intraoperatively, particularly during manipulation of the tumor; it is probably wise to include glucose in intravenously administered fuids.

THYROID DISEASE

Te recurrent laryngeal nerve and external motor branch of the superior laryngeal nerve are in intimate proximity to the gland.

The T4/T3 ratio of secreted hormones is 10:1.

Although only 10% of thyroid hormone secretion is T3, T3 is three to four times more active than T4

Tyroid hormone acts directly on cardiac myocytes and vascular smooth muscle cells.that are important for systolic contractile function and diastolic relaxation

Tyroid hormone increases myocardial contractility directly, decreases systemic vascular resistance via direct vasodilation, and increases intravascular volume.

Diagnosis The third generation of the TSH assay

normal level of TSH is 0.4 to 5.0 milliunits/L. A

TSH level of 0.1 to 0.4 milliunits/L with normal levels of free

T3 (FT3) and free T4 (FT4) is diagnostic of subclinical hyperthyroidism.

TSH level of less than 0.03 milliunits/L with elevated T3 and T4 is diagnostic of overt hyperthyroidism.

TSH level of 5.0 to 10 milliunits/L with normal levels of FT3 and FT4 is diagnostic of subclinical hypothyroidism.

TSH level of more than 20 milliunits/L (may be as high as 200 or even 400 milliunits/L) with reduced levels of T3 and T4 is diagnostic of overt hypothyroidism.

Hyperthyroidism SIGNS AND SYMPTOMS

3 majority of cases of hyperthyroidism:

1. Graves' disease

2. toxic multinodular goiter

3. toxic adenoma.

patient is anxious, restless, and hyperkinetic and may be emotionally unstable.

skin is warm and moist, the face is fushed, the hair is fine, and the nails are soft and fragile, increased sweating and complain of heat intolerance.

Elderly patients with unexplained cardiac failure or rhythm disturbances— especially atrial in origin—should be evaluated for thyrotoxicosis.

exophthalmos or proptosis resulting from an infltrative

process that involves retrobulbar fat and the eyelids

Wasting, weakness, and fatigue are common.

tachycardia, arrhythmias and palpitations, increased myocardial contractility and cardiac output, and cardiomegaly.

Graves' disease

occurs in 0.4% of the U.S.

female/male ratio is 7:1

ages of 20 and 40 years.

Graves' disease appears to be a systemic autoimmune

disease caused by thyroid-stimulating antibodies that bind to TSH receptors in the thyroid

graves:

ophthalmopathy occurs in 30% +dermopathy+hyperthyroidism

Toxic multinodular form simple goiter and

occurs mostly in patients older than 50 years of age.

It may present with extreme thyroid enlargement that can cause dysphagia, globus sensation, and possibly inspiratory stridor from tracheal compression.

mass extends into the thoracic inlet behind the sternum. In severe cases, superior vena cava obstruction syndrome may also be present.

TREATMENT

methimazole or propylthiouracil (PTU).

PTU has the added advantage of inhibiting the peripheral conversion of T4 to T3.

A euthyroid state achieved in 6 to 8 weeks

Side efects (3% to 12%) agranulocytosis

β-Adrenergic antagonists relieve signs and symptoms such as anxiety, sweating, heat intolerance, tremors, and tachycardia.

Propranolol affect the peripheral conversion of T4 to T3

surgery include hypothyroidism, hemorrhage with tracheal Complications from compression, unilateral or bilateral damage to the recurrent laryngeal nerve(s), damage to the motor branch of the superior laryngeal nerve, and damage to or inadvertent removal of the parathyroid glands

Hyperthyroidism during pregnancy is treated with low dosages of antithyroid drugs.

If dosages higher than 300 mg/day of PTU are needed during the frst trimester, a subtotal thyroidectomy should be performed in the second trimester.

cross the placenta and can cause fetal hypothyroidism.

MANAGEMENT OF ANESTHESIA

In hyperthyroid patients undergoing surgery, euthyroidism should defnitely be established preoperatively. 6 to 8 weeks

In emergency cases, the use of an intravenous β-blocker, glucocorticoids, and PTU is usually necessary.

Glucocorticoids (dexamethasone 2 mg IV every 6 hours) should be administered to decrease hormone release and reduce the peripheral conversion of T4 to T3.

Evaluation of the upper airway for evidence of tracheal compression or deviation caused by a goiter is an important part of the preoperative evaluation

Examination of chest radiographs and CT scans is ofen helpful .

Establishment of adequate anesthetic depth is extremely important to avoid exaggerated sympathetic nervous system responses.

Drugs that stimulate the sympathetic nervous system (i.e., ketamine, pancuronium, atropine, ephedrine, epinephrine)

should be avoided.

Tiopental,decreases the peripheral conversion of T4 to T3 and may have a slight advantage over other agents for anesthesia induction.

maintenance of anesthesia, any of the potent inhalation agents may be used.

Hyperthyroid patients may have co-existing muscle disease (e.g.myasthenia gravis) with reduced requirements for the nondepolarizing muscle relaxants; therefore, careful titration is required.

For the treatment of intraoperative hypotension, a direct-acting vasopressor (phenylephrine) is preferred. Ephedrine, epinephrine, norepinephrine, and dopamine should be avoided or administered in extremely low doses to prevent exaggerated hemodynamic responses.

Epinephrine containing local anesthetic solutions should be avoided.

Removal of the thyrotoxic gland does not mean immediate resolution of thyrotoxicosis. The half-life of T4 is 7 to 8 days; therefore, β-blocker therapy may need to be continued in the postoperative period

THYROID STORM

Tyroid storm is a life-threatening exacerbation of hyperthy-

roidism precipitated by trauma, infection, medical illness, or surgery.

Tyroid storm and malignant hyperthermia

The cause is probably a shift from protein-bound thyroid hormone to free hormone as a result of the presence of circulating inhibitors to binding.

Tyroid storm most ofen occurs in the postoperative period in untreated or inadequately treated hyperthyroid patients afer emergency surgery.

extreme anxiety, fever, tachycardia, cardiovascular instability, and altered consciousness .

Treatment includes rapid alleviation of thyrotoxicosis and general supportive care.

Dehydration is managed with intravenous administration of glucose-contain-ing crystalloid solutions, and cooling measures (e.g., cooling blanket, ice packs, administration of cool humidifed oxygen) are used to counter the fever.

β-Blockers should be titrated to decrease heart rate to less than 90 beats per minute.

Dexamethasone 2 mg every 6 hours or cortisol 100 to 200 mg every 8 hours can be used to decrease hormone release and conversion of T4 to T3.

Antithyroid drugs (PTU 200 to 400 mg every 8 hours) may be administered through a nasogastric tube, orally, or rectally.

If circulatory shock is present, intravenous administration of a direct vasopressor (phenylephrine) is indicated.

Hypothyroidism

SIGNS AND SYMPTOMS

0.5% to 0.8% of the adult population

most common cause in ablation of the gland by radioactive iodine or surgery. second type idiopathic and probably autoimmune

In mild cases, patients weight gain. :fatigue, lethargy, apathy, and listlessness. speech becomes slow

,cold intolerance, decreased sweating, constipation, menorrhagia, and slowing of motor function.

cardiac output is decreased secondary to reductions in stroke volume and heart rate. Baroreceptor function is also impaired

sinus bradycardia; ventricular dysrhythmias may also be

present.Peripheral vascular resistance is increased and blood

volume is reduced, which results in pale, cool skin.

Pericardial efusions are common.

Hyponatremia and impairment of free water excretion are also common, related to inappropriate secretion of antidiuretic hormone (ADH).

Maximum breathing capacity and difusion capacity are decreased, and ventilatory responsiveness to hypoxia and hypercarbia is depressed.

Pleural efusions may result in dyspnea.

adynamic ileus may occur. Deep tendon refexes demonstrate a prolonged relaxation phase.

TREATMENT

l-Tyroxine (levothyroxine sodium) is usually administered for the treatment of hypothyroidism.

MANAGEMENT OF ANESTHESIA

patients can be extremely sensitive to narcotics and sedatives and may even be lethargic secondary to their disease; therefore, preoperative sedation should be undertaken with caution.Airway compromise

Decreased gastric emptying increases the risk of

regurgitation and aspiration.

A hypodynamic cardiovascular system characterized by decreased cardiac output, stroke volume, heart rate, baroreceptor refexes, and intravascular volume may be compromised by surgical stress and cardiac-depressant anesthetic agents.

Decreased ventilatory responsiveness to hypoxia and hypercarbia is enhanced by anesthetic agents.

Hypothermia occurs quickly and is difcult to treat.

Hematologic abnormalities such as anemia (25% to 50% of patients) and dysfunction of platelets and coagulation factors especially factor VIII), electrolyte imbalances (hyponatremia), and hypoglycemia are common and require close monitoring intraoperatively.

Decreased neuromuscular excitability is exacerbated by anesthetic drugs.

Hypothyroid patients also appear to have an increased sensitivity to anesthetic drugs, although the efect of thyroid activity on the minimum alveolar concentration of volatile anesthetics is negligible.

Increased sensitivity is probably secondary to reduced cardiac output, decreased blood volume, abnormal baroreceptor function, decreased hepatic metabolism, and decreased renal excretion of drugs.

Hypothyroid patients are very sensitive to the myocardial-depressant efects of the potent inhalational agents.

Vasodilation in the presence of possible hypovolemia and impaired baroreceptor activity can produce signifcant hypotension.

Pharmacologic support for intraoperative hypotension is best provided with ephedrine, dopamine, or epinephrine and not a pure α-adrenergic agonist (phenylephrine). Unresponsive hypotension may require supplemental steroid administration.

Dextrose in normal saline is the recommended intravenous fuid to avoid hypoglycemia and minimize hyponatremia secondary to impaired free water clearance.

MYXEDEMA COMA

Myxedema coma is a rare severe form of hypothyroidism characterized by delirium or unconsciousness, hypoventilation, hypothermia (80% of patients), bradycardia, hypotension, and a severe dilutional hyponatremia.

It occurs most commonly in elderly women with a long history of hypothyroidism. Infection, trauma, cold, and central nervous system depressants predispose hypothyroid patients to myxedema coma.

Myxedema coma is a medical emergency with a mortality rate higher than 50%.

Intravenous l-thyroxine or l-triiodothyronine is the treatment of choice. Intravenous hydration with glucose-containing saline solutions, temperature regulation, correction of electrolyte imbalances, and stabilization of the cardiac and pulmonary systems are necessary.

Mechanical ventilation is frequently required.

Hydrocortisone 100 to 300 mg/day IV is also prescribed to treat possible adrenal insufciency.

Goiter and Thyroid Tumors

A goiter is a swelling of the thyroid gland that results from compensatory hypertrophy and hyperplasia of follicular epithelium secondary to a reduction in thyroid hormone output

In most cases, a goiter is associated with a euthyroid state,

.Surgery is indicated only if medical therapy is inefective and the goiter is compromising the airway or is cosmetically unacceptable.

Examination of a CT scan of the neck will demonstrate anatomic abnormalities.

sedatives and narcotics should be avoided or used with great caution before and during endotracheal tube placement.

Awake intubation is the safest method to assess the degree of obstruction and establish the airway.

Surgical removal of the mass may reveal underlying tracheomalacia and a collapsible airway.

Tracheal extubation should be performed with as much caution and concern as intubation.

If the mass extends into the substernal regional (i.e., ante-

rior mediastinal mass), superior vena cava obstruction, major airway obstruction, and/or cardiac compression may occur.

During spontaneous respiration, the larger airways are

supported by negative intrathoracic pressure, and the efects of extrinsic compression may be apparent in only the most severe cases.

With cessation of spontaneous respiration, com-

pensatory mechanisms are removed and airway obstruction occurs. In addition, positive pressure ventilation may demonstrate total airway occlusion

A preoperative history of dyspnea in the upright or supine position is predictive of possible airway obstruction during general anesthesia.

A CT scan must be examined to assess the extent of the tumor

Echocardiography with the patient in the upright and supine positions can indicate the degree of cardiac compression.

If practical, local anesthesia is recommended for patients

requiring surgery.

If general anesthesia is necessary,

In such patients, an awake intubation with fberoptic bronchoscopy using an anode tube is

recommended. The patient is placed in semi-Fowler's position, and volatile anesthetic with nitrous oxide and oxygen is administered using spontaneous ventilation. Muscle relaxants are avoided.

It must be possible to change the patient's position.

Following tumor resection, the airway should be exam-

ined by fberoptic bronchoscopy to detect tracheomalacia and determine whether and when tracheal extubation is appropriate.

A rigid bronchoscope should be available to reestablish

the airway if collapse occurs.

Cardiopulmonary bypass equipment should be on standby during the case.

Complications of Thyroid Surgery

Morbidity from thyroid surgery approaches 13%

Recurrent laryngeal nerve injury may be unilateral or bilateral and temporary or permanent.

Hypoparathyroidism is also a complication of thyroid surgery

The signs and symptoms of hypocalcemia occur in the frst 24 to 48 hours postoperatively. Anxiety, circumoral numbness, tingling of the fingertips, muscle cramping, and positive Chvostek's and Trousseau's signs are indicative of hypocalcemia.

stridor can occur and can proceed to laryngospasm.

Immediate treatment with intravenous calcium gluconate (1 g, 10 mL of a 10% solution) or calcium chloride (1 g, 10 mL of a 10% solution) is necessary.

Tracheal compression from an expanding hematoma may

cause rapid respiratory compromise in the period immediately afer thyroid surgery.

Immediate hematoma evacuation is the frst line of treatment. If time permits, the patient should

be returned to the operating room. If necessary, the wound should be opened at the bedside, clots evacuated, and bleeding vessels secured to relieve airway obstruction.

PHEOCHROMOCYTOMA

Pheochromocytomas are catecholamine-secreting tumors that arise from chromafn cells of the sympathoadrenal system.

Uncontrolled catecholamine release can result in malignant hypertension, cerebrovascular accident, and myocardial infarction.

Familial pheochromocytomas can also be part of the MEN 2

Most pheochromocytomas secrete norepinephrine,or combination with a smaller amount of epinephrine

Signs and Symptoms

the clinical presentation of pheochromocytoma is variable

Headache, sweating, pallor, and palpitations are other classic signs and symptoms.

Orthostatic hypotension is also a common fnding and is considered to be secondary to hypovolemia and impaired vasoconstrictor reflex responses.

Hemodynamic signs depend on the predominant catecholamine secreted. With norepinephrine, α-adrenergic efects predominate, and patients usually have systolic and diastolic hypertension and a refex bradycardia.

With epinephrine, β-adrenergic efects predominate, and patients usually have systolic hypertension, diastolic hypotension, and tachycardia.

Cardiomyopathy is a complication of pheochromocytoma.

Both dilated and hypertrophic cardiomyopathies, as well as lef ventricular outfow tract obstruction, have been demonstrated echocardiographically.

ECG abnormalities may include elevation or depression of the ST segment, fattening or inversion of T waves, prolongation of the QT interval, high or peaked P waves, left axis deviation, and arrhythmias.

Management of Anesthesia

PREOPERATIVE MANAGEMENT

Since most pheochromocytomas secrete predominantly norepinephrine, medical therapy has depended on α-blockade to lower blood pressure, increase intravascular volume, prevent paroxysmal hypertensive episodes, allow resensitization of adrenergic receptors, and decrease myocardial dysfunction.

Phenoxybenzamine :It is a noncompetitive α1-antagonist with some α2-blocking properties.

The goal of therapy is normotension, a resolution of symptoms, elimination of ST-segment and T-wave changes on the ECG, and elimination of arrhythmias.

Overtreatment can result in severe orthostatic hypotension.

The optimal duration of α-blockade therapy is undetermined and may range from 3 days to 2 weeks or longer.

Because of the prolonged effect of phenoxybenzamine on α-receptors, the recommendation has been to discontinue its use 24 to 48 hours before surgery to avoid vascular unresponsiveness immediately following removal of the tumor.

Prazosin and doxazosin, pure α1-competitive blockers, are alternatives to phenoxybenzamine. They are shorter acting, cause less tachycardia.

A nonselective β-blocker should never be administered before α-blockade, because blockade of vasodilatory β2-receptors results in unopposed α-agonism, leading to vasoconstriction and hypertensive crises.

Propranolol, a nonselective β-blocker with a half-life longer than 4 hours, is most frequently used pheochromocytoma patients.

Esmolol has a fast onset and short elimination half-life and can be administered intravenously in the period immediately before surgery.

α-Methylparatyrosine (metyrosine) It is especially useful for malignant and inoperable tumors.

INTRAOPERATIVE MANAGEMENT

Optimal prepration :α-adrenergic blocker with or without a β-blocker with αmethylparatyrosine, correction of hypovolemia.

Intraoperative goals Hypertension frequently occurs during pneumo-

peritoneum as well as during tumor manipulation. On the other hand, signifcant hypotension may develop following ligation of the tumor's venous drainage.

invasive monitoring methods

transesophageal echocardiography may be necessary to manage the large fuid requirements, major volume shifs, and possible underlying myocardial dysfunction in patients with very active tumors.

Factors that stimulate catecholamine release such as fear,stress, pain, shivering, hypoxia, and hypercarbia must be minimized in the perioperative period.

Morphine and atracurium can cause histamine release, which may provoke release of catecholamines from the tumor. Atropine, pancuronium, and succinylcholine are examples of vagolytic or sympathomimetic

drugs that may stimulate the sympathetic nervous system.

systolic arterial pressure in excess of 200 mm Hg Sodium nitroprusside, a direct vasodilator, is the agent of choice because of its potency, immediate onset of action, and short duration of action.

Phentolamine, a competitive α-adrenergic blocker and a direct vaso-dilator, is efective, although tachyphylaxis and tachycardia are associated with its use.

Nitroglycerin is efective, but large doses are ofen required and may cause tachycardia.

Labetalol, with more β- than α-blocking properties, is preferred for predominantly epinephrine-secreting tumors.

Magnesium sulfate inhibits release of catecholamines from the adrenal medulla and peripheral nerve terminals, reduces sensitivity of α-receptors to catecholamines, is a direct vasodilator, and is an antiarrhythmic.

Increasing the depth of anesthesia is also an option

Arrhythmias are usually ventricular in origin and are managed with either lidocaine or β-blockers.

Amiodarone, an antiarrhythmic agent that prolongs the duration of the action potential of atrial and ventricular muscle, has been used as an alternative to β-blockers to treat supraventricular

tachycardia associated with hypercatecholaminemia.

Lactated Ringer's solution and physiologic saline are the recommended fuids for use before tumor removal.

insulin levels increase and hypoglycemia may occur. Terefore, dextrose-containing solutions should be added afer tumor removal.

Glucocorticoid therapy should be administered if a bilateral adrenalectomy is performed or if hypoadrenalism is a possibility